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PubMed1992

Pseudomonas pseudomallei liver abscesses: a clinical, laboratory, and ultrasonographic study.

Ultrasonography revealed evidence of liver abscess in 126 patients who were admitted to one hospital in northeastern Thailand over a 3-year period. There were 50 cases for which a pyogenic bacterial etiology was confirmed; 34 cases (group 1) were caused by Pseudomonas pseudomallei (nine patients died) and 16 cases (group 2) were caused by other bacteria (two patients died). Melioidosis was associated with anemia and underlying diabetes or renal disease; right-upper-quadrant pain and jaundice were more common in group 2 (P less than .05). Blood cultures were positive for bacteria in 68% of group 1 and 50% of group 2. Chest radiographs revealed abnormalities in 17 of 30 group 1 patients and 6 of 12 group 2 patients. The radiographic appearances of a blood-borne pneumonia suggested melioidosis. The serum indirect hemagglutination assay for antibodies to P. pseudomallei was of limited value in differentiating the two types of abscesses. Multiple hypoechoic areas on ultrasonography were significantly associated with melioidosis (P less than .01); associated splenic abscess occurred in 19 group 1 patients but only one group 2 patient (2-107, 95% confidence interval; odds ratio, 19). In an area where P. pseudomallei is endemic, these characteristic ultrasonographic findings should prompt immediate treatment for melioidosis.

Adolescent↗
PubMed1989

Acute suppurative parotitis caused by Pseudomonas pseudomallei in children.

During a prospective clinical study of melioidosis in northeast Thailand, suppurative parotitis was observed as a characteristic presentation in children. Parotitis constituted 6.3% of all culture-positive melioidosis and 38% of melioidosis in children. Nine cases are described. None had apparent predisposition to infection, although two patients developed rising mumps virus antibody titers, suggesting a possible relation between these conditions. Complications included abscess formation (nine), spontaneous rupture into the auditory canal (five), facial nerve palsy (two), and septicemia and osteomyelitis with septic arthritis (one each). All children initially responded to surgical drainage and appropriate antibiotic therapy. Pseudomonas pseudomallei parotitis should be considered in children from endemic areas with fever and facial swelling. It has a good prognosis with appropriate treatment. It may also prove to be a sensitive clinical indicator of the presence of melioidosis within a particular geographic area.

Abscess↗
PubMed1999

Rapid identification of Burkholderia pseudomallei in blood cultures by latex agglutination using lipopolysaccharide-specific monoclonal antibody.

Melioidosis, an infection caused by Burkholderia pseudomallei, is endemic in Southeast Asia. The septicemic form of melioidosis is the leading cause of death due to community-acquired bacteremia in the northeastern part of Thailand. The delay in isolation and identification of the causative organism is a major contributing factor to the high mortality. The present study describes the evaluation of a latex agglutination test for rapid identification of the bacteria directly from blood cultures. The Bps-L1 monoclonal antibody recognized the lipopolysaccharide antigen of 96.8% of B. pseudomallei clinical isolates and was highly specific for B. pseudomallei. The diagnostic value of the latex agglutination test based on Bps-L1 monoclonal antibody was prospectively evaluated in an area endemic for melioidosis. The agglutination test kit was evaluated in 88 blood cultures with gram-negative bacteria identified with Gram staining. The sensitivity and specificity of the test kit were both 100%. These results indicated that the detection of B. pseudomallei lipopolysaccharide by specific monoclonal antibody in a latex agglutination format is clinically useful for the rapid identification of the bacteria in blood cultures in areas endemic for melioidosis.

Animals↗
PubMed1999

Epidemiology of arabinose assimilation in burkholderia pseudomallei isolated from patients and soil in Thailand.

Burkholderia pseudomallei is an environmental saprophyte that has been isolated widely from soil in Southeast Asia and the relationship between environmental contamination and clinical melioidosis has been established. It has been shown that the arabinose assimilation property of B. pseudonrallei is probably one of the determinants indicating virulence of this organism. Therefore, the distribution of arabinose assimilation biotypes of B. pseudomallei collected from four geographic regions of Thailand was studied in order to determine an association between arabinose assimilation of B. pseudomallei and the uneven distribution of melioidosis found among these four areas. A total of 830 isolates of B. pseudomallei (412 patient isolates and 418 soil isolates) collected from the patients and soil in four regions of Thailand in 1997 were tested for an ability to grow on a minimal agar medium supplemented with L-arabinose. All patient isolates except one could not utilise arabinose (Ara-). For 418 soil isolates, 232 (55.5%) isolates were identified as Ara type. They comprised 180 (62.5%), 36 (46.8%), 6 (35.3%) and 10 (27.8%) isolates derived from northeastern, southern, northern and central regions respectively. The ratios of Ara- to Ara, were 1.7, 0.9. 0.5 and 0.4 among isolates collected from northeastern, southern, northern and central regions respectively. The prevalence of Ara- in soil isolates in northeast is significantly higher than those in other regions. This observation suggests that in addition to the presence of B. pseudomallei in soil which is one of the factors contributing to a burden of melioidosis in northeastern Thailand, the distribution of more virulent biotype (Ara-) soil isolates is a factor contributing to a high prevalence of melioidosis in northeastern Thailand as well.

Arabinose↗
PubMed1980

Meliodosis.

During the five-month wet season of 1977-1978 in Northern Queensland, six patients with bacteriologically proven melioidosis were successfully treated at the Townsville General Hospital, The clinical course and management of each case and laboratory findings are described. Factors which predisposed them to infection with Pseudomonas pseudomallei were diabetes mellitus, cancer, alcoholism, malnutrition, trauma, and pregnancy. Successful treatment of melioidosis relied on prompt laboratory diagnosis and appropriate chemotherapy together with surgical drainage of abscesses and management of concomitant diseases. The incidence of melioidosis in Northern Queensland has increased to the extent that it can no longer be considered a rare disease in this area. Because of increased internal and international travel, and displacement of refugees from endemic areas of Southeast Asia, physicians and microbiologists must maintain a high index of suspicion of melioidosis when dealing with patients after geographic exposure, as it is probable that, in the future, this disease witll be encountered more frequently in non-endemic areas.

Adult↗
PubMed1997

In-vitro susceptibility of Burkholderia pseudomallei to cefoperazone-sulbactam combination.

Melioidosis is endemic in Malaysia. Emerging resistance with new and current antimicrobial agents has underscored the need to look further for new antimicrobial agents for the treatment of melioidosis. Hence, we evaluated the in-vitro susceptibility of fifty locally isolated strains of Burkholderia pseudomallei, the causative agent of melioidosis to cefoperazone-sulbactam combination using the method of NCCLS. All the fifty strains tested were susceptible in-vitro to cefoperazone-sulbactam. The MIC90 of the organism for cefoperazone-sulbactam was 4 mg/L. The results of our findings suggested that cefoperazone-sulbactam may be useful in the treatment of melioidosis.

Burkholderia pseudomallei↗
PubMed1976

A retrospective serological suvey of Royal Marines previously exposed to Pseudomonas pseudomallei in South East Asia.

Following the suggestion that it was possible that cases of melioidosis amongst those who had been exposed abroad in the past, might be escaping notice, 487 Royal Marines were examined by indirect haemagglutination studies. Four hundred and eleven of these subjects had served for variable times in areas where melioidosis has been known to occur in Indonesia and Malaya, between 1960 and 1974, occupied in activities in the jungle and paddy fields during which exposure to the disease was to be expected. No evidence of residual subclinical melioidosis was found and it seems unlikely that recrudescent disease will prove to be a problem in the future for English servicemen who have been in South East Asia.

Antibodies, Bacterial↗
PubMed2005

Kinetic studies of bioactive products nitric oxide and 8-iso-PGF(2alpha) in Burkholderia pseudomallei infected human macrophages, and their role in the intracellular survival of these organisms.

The oxidative response of Burkholderia pseudomallei and Escherichia coli infected macrophages from normal and melioidosis subjects was determined by measuring the production of nitric oxide which is one of the reactive nitrogen intermediates, and the activation state of these macrophages was determined by measuring the generation of 8-iso-PGF(2alpha), a bioactive product of free radical induced lipid peroxidation. Macrophages obtained from the melioidosis patients generated significantly lower levels of nitric oxide and 8-iso-PGF(2alpha) compared to macrophages obtained from the normal subjects (P<0.001). The reduced efficiency of the oxygen dependent microbicidal mechanism in macrophages of melioidosis patients may be one of the survival strategies developed by B. pseudomallei to remain viable intracellularly.

Burkholderia pseudomallei↗
PubMed2005

Decreased protein C, protein S, and antithrombin levels are predictive of poor outcome in Gram-negative sepsis caused by Burkholderia pseudomallei.

BACKGROUND: Acute septicemic melioidosis is associated with systemic release of endotoxin and the proinflammatory cytokines tumor necrosis factor (TNF)-alpha, interleukin-1, and interleukin-6. Excessive release of these cytokines may lead to endothelial injury, depletion of naturally occurring endothelial modulators, microvascular thrombosis, organ failure, and death. METHOD: Plasma samples drawn at baseline and after initial antimicrobial therapy in 30 patients with suspected acute severe melioidosis were assayed for D-dimer levels, protein C and protein S antigen levels, and antithrombin functional activities. RESULTS: Both baseline and continued deficiencies of protein C, protein S, and antithrombin were statistically associated with a poor outcome by logistic regression. Baseline D-dimer levels were significantly higher in fatal cases than survivors and correlated inversely with protein C and antithrombin, suggesting both increased fibrin deposition and fibrinolysis. CONCLUSION: The inflammatory response to systemic Burkholderia pseudomallei infection leads to depletion of the natural endothelial modulators protein C, protein S, and antithrombin. Both baseline and continued deficiency of these endothelial modulators is predictive of poor outcome in melioidosis.

Adult↗
PubMed2006

Six cases of suppurative lymphadenitis caused by Burkholderia pseudomallei infection.

Melioidosis, an infection caused by Burkholderia pseudomallei, is endemic in Southeast Asia and northern Australia. It can have various presentations, ranging from acute septicaemia to chronic localized infection. Uncomplicated, localized infection usually involves skin or subcutaneous tissues. Suppurative lymphadenitis caused by melioidosis has been rarely encountered by clinicians practicing in endemic areas. We encountered six cases of suppurative lymphadenitis caused by Burkholderia pseudomallei in adults who were admitted to hospital in Singapore from 1997 to 2000. The most striking difference between these patients and cases reported previously was the pattern of the lymph node involvement. In the majority of previously described patients the infected lymph nodes were in the head and neck region. By contrast, four patients in our study presented with unilateral, inguinal lymphadenitis. Another two patients presented with mediastinal lymphadenitis and prolonged fever. All patients had prompt and sustained response to therapy. Melioidosis should be considered in the differential diagnosis of suppurative, regional lymphadenitis, especially in patients who travelled to, or stayed in, an endemic area.

Adolescent↗
PubMed2000

Ecology of Burkholderia pseudomallei and the interactions between environmental Burkholderia spp. and human-animal hosts.

Early workers thought that melioidosis was a zoonosis with a reservoir in rodents, but we now know that Burkholderia pseudomallei is a widely distributed environmental saprophyte. In northeast Thailand, two thirds of paddy fields yield the organism, and 80% of children have antibodies by the time they are 4 years old. However, interpretation of these results has been complicated by the recent recognition of avirulent, antigenically cross-reacting environmental organisms for which the name B. thailandensis has been proposed. We still know very little about the climatic, physical, chemical and biological factors which control the proliferation and survival of Burkholderia spp. in the environment, although epidemiological studies show space-time clustering of melioidosis. It is assumed that most human and animal melioidosis arises through exposure to contaminated soil or muddy water, although only 6% of human cases have a clear history of inoculation, and a further 0.5% of cases follow near-drowning. Laboratory animals have also been infected by ingestion, inhalation and insect bites, but evidence of infection acquired naturally by these routes remains anecdotal. Sporadic cases have resulted from iatrogenic inoculation, laboratory accidents, and person-to-person or animal-to-person spread. Whether exposure to B. pseudomallei will result in disease probably depends on the balance between the virulence of the strain, the immune status of the host (e.g. diabetes mellitus) and the size of the inoculum.

Animals↗
PubMed2000

Proinflammatory cytokine mRNA responses in experimental Burkholderia pseudomallei infection in mice.

Melioidosis is a potentially fatal disease of both human and animals caused by the bacterium Burkholderia pseudomallei. Disease is endemic in tropical and subtropical regions of Southeast Asia and Northern Australia. The pathogenesis of melioidosis is poorly understood. In particular, the host responses that occur following infection, and the specific host-pathogen interactions that result in the development of either acute or chronic infection are unclear. Using an established murine model, we investigated early proinflammatory cytokine responses believed to be critical in the development of acute and chronic B. pseudomallei infection. Semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) was used to assess levels of mRNA for tumor necrosis factor-alpha (TNF-alpha), interleukin 1beta (IL-1beta) and interleukin 6 (IL-6) in the liver of mice following infection. We demonstrate that the level of mRNA for these cytokines increase moderately in chronic infection in C57BL/6 mice. However, in acute infection in BALB/c mice, mRNA responses for these cytokines were shown to be comparatively greater. These results demonstrate that early proinflammatory cytokine responses are important in the immunopathogenesis of melioidosis.

Animals↗
PubMed2006

Pyogenic liver abscess caused by Burkholderia pseudomallei in Taiwan.

Pyogenic liver abscess in Taiwan is a well-known disease entity, commonly associated with a single pathogen, Klebsiella pneumoniae. Melioidosis is an endemic disease in Taiwan that can manifest as multiple abscesses in sites including the liver. We report three cases of liver abscesses caused by Burkholderia pseudomallei. The first patient was a 54-year-old diabetic woman, who presented with liver abscess and a left subphrenic abscess resulting from a ruptured splenic abscess, co-infected with K. pneumoniae and B. pseudomallei. The second patient, a 58-year-old diabetic man, developed bacteremic pneumonia over the left lower lung due to B. pseudomallei with acute respiratory distress syndrome, and relapsed 5 months later with bacteremic abscesses of the liver, spleen, prostate and osteomyelitis, due to lack of compliance with prescribed antibiotic therapy. The third patient was a 61-year-old diabetic man with a history of travel to Thailand, who presented with jaundice and fever of unknown origin. Liver and splenic abscesses due to B. pseudomallei were diagnosed. A high clinical alertness to patients' travel history, underlying diseases, and the presence of concomitant splenic abscess is essential to early detection of the great mimicker, melioidosis. The treatment of choice is intravenous ceftazidime for at least 14 days or more. An adequate duration of maintenance oral therapy, with amoxicillin-clavulanate or trimethoprim-sulfamethoxazole for 12-20 weeks, is necessary to prevent relapse. Liver abscess in Taiwan is most commonly due to K. pneumoniae, but clinicians should keep in mind that this may be a presenting feature of melioidosis.

Anti-Bacterial Agents↗
PubMed2001

Burkholderia pseudomallei virulence: definition, stability and association with clonality.

Clinical presentations of melioidosis, caused by Burkholderia pseudomallei are protean, but the mechanisms underlying development of the different forms of disease remain poorly understood. In murine melioidosis, the level of virulence of B. pseudomallei is important in disease pathogenesis and progression. In this study, we used B. pseudomallei-susceptible BALB/c mice to determine the virulence of a library of clinical and environmental B. pseudomallei isolates from Australia and Papua New Guinea. Among 42 non-arabinose-assimilating (ara(-)) isolates, LD(50) ranged from 10 to > 10(6) CFU. There were numerous correlations between virulence and disease presentation in patients; however, this was not a consistent observation. Virulence did not correlate with isolate origin (i.e. clinical vs environmental), since numerous ara(-) environmental isolates were highly virulent. The least virulent isolate was a soil isolate from Papua New Guinea, which was arabinose assimilating (ara(+)). Stability of B. pseudomallei virulence was investigated by in vivo passage of isolates through mice and repetitive in vitro subculture. Virulence increased following in vivo exposure in only one of eight isolates tested. In vitro subculture on ferric citrate-containing medium caused attenuation of virulence, and this correlated with changes in colony morphology. Pulsed-field gel electrophoresis and randomly amplified polymorphic DNA typing demonstrated that selected epidemiologically related isolates that had variable clinical outcomes and different in vivo virulence were clonal strains. No molecular changes were observed in isolates after in vivo or in vitro exposure despite changes in virulence. These results indicate that virulence of selected B. pseudomallei isolates is variable, being dependent on factors such as iron bioavailability. They also support the importance of other variables such as inoculum size and host risk factors in determining the clinical severity of melioidosis.

Animals↗
PubMed1998

The type II O-antigenic polysaccharide moiety of Burkholderia pseudomallei lipopolysaccharide is required for serum resistance and virulence.

Melioidosis, an infection caused by the gram-negative bacterial pathogen Burkholderia pseudomallei, is endemic in south-east Asia and northern Australia. Acute septicaemic melioidosis is a major cause of morbidity and mortality, especially in north-east Thailand. B. pseudomallei is highly resistant to the bactericidal activity of normal human serum (NHS), and we have found that B. pseudomallei 1026b multiplies in 10-30% NHS. We developed a simple screen for the identification of serum-sensitive mutants based on this novel phenotype. Approximately 1200 Tn5-OT182 mutants were screened, and three serum-sensitive mutants were identified. The type II O-antigenic polysaccharide (O-PS) moiety of lipopolysaccharide was not present in the serum-sensitive mutants. A representative serum-sensitive mutant, SRM117, was killed by the alternative pathway of complement and was less virulent than 1026b in three animal models of melioidosis. The Tn5-OT182 integrations in the serum-sensitive mutants were physically linked on the B. pseudomallei chromosome, and further genetic analysis of this locus revealed a cluster of 15 genes required for type II O-PS production. The proteins encoded by these genes were similar to proteins involved in bacterial polysaccharide biosynthesis. The results presented here demonstrate that type II O-PS is essential for B. pseudomallei serum resistance and virulence.

1-Acylglycerol-3-Phosphate O-Acyltransferase↗
PubMed2001

Induction of multiple chemokine and colony-stimulating factor genes in experimental Burkholderia pseudomallei infection.

Melioidosis is a disease of the tropics caused by the facultative intracellular bacterium Burkholderia pseudomallei. In human infection, increased levels of IFN-gamma in addition to the chemokines interferon-gamma-inducible protein 10 (IP-10) and monocyte interferon-gamma-inducible protein (Mig) have been demonstrated. However, the role of these and other chemokines in the pathogenesis of melioidosis remains unknown. Using BALB/c and C57BL/6 mice as models of the acute and chronic forms of human melioidosis, the induction of mRNA was assessed for various chemokines and CSF (G-CSF, M-CSF, GM-CSF, IP-10, Mig, RANTES, MCP-1, KC and MIP-2) in spleen and liver following B. pseudomallei infection. Patterns of chemokine and CSF induction were similar in liver and spleen; however, responses were typically greater in spleen, which reflected higher tissue bacterial loads. In BALB/c mice, high-level expression of mRNA for all chemokines and CSF investigated was demonstrated at day 3 postinfection, correlating with peak bacterial load and extensive infiltration of leucocytes. In contrast, increased mRNA expression and bacterial numbers in C57BL/6 mice were greatest between 4 and 14 days following infection. This paralleled increases in the size and number of abscesses in liver and spleen of C57BL/6 mice at days 3 and 14 postinfection. Earlier induction of cytokine-induced neutrophil chemoattractant (KC), macrophage inflammatory protein-2 (MIP-2), monocyte chemoattractant protein-1 (MCP-1), granulocyte-macrophage CSF (GM-CSF) and macrophage CSF (M-CSF) mRNA was demonstrated in spleen, while MIP-2, MCP-1, IP-10 and Mig were demonstrated in liver of BALB/c mice when compared to spleen and liver of C57BL/6. The magnitude of cellular responses observed in the tissue correlated with increased levels of the chemokines and CSF investigated, as well as bacterial load. Compared with C57BL/6 mice, greater infiltration of neutrophils was observed in liver and spleen of BALB/c mice at day 3. In contrast, early lesions in C57BL/6 mice predominantly comprised macrophages. These results suggest that the inability of BALB/c mice to contain the infection at sites of inflammation may underlie the susceptible phenotype of this mouse strain towards B. pseudomallei infection.

Animals↗
PubMed1998

Burkholderia pseudomallei infection in a Puerto Rican patient with chronic granulomatous disease: case report and review of occurrences in the Americas.

Burkholderia species, notably Burkholderia cepacia and Burkholderia gladioli, are important pathogens in patients with chronic granulomatous disease (CGD). Burkholderia pseudomallei, the causative agent of melioidosis, is endemic in Southeast Asia and northern Australia but is a rare pathogen in other parts of the world. We describe the occurrence of B. pseudomallei infection in a Puerto Rican patient with CGD. This is one of only a small number of documented cases of melioidosis autochthonous to the Americas and is the first reported case of B. pseudomallei infection in a CGD patient from the Americas. We conclude that B. pseudomallei, like B. cepacia and B. gladioli, should be considered a potential pathogen in patients with CGD and that melioidosis should be considered in the differential diagnosis for ill residents of or travelers to Puerto Rico.

Americas↗
PubMed1993

Serology and carriage of Pseudomonas pseudomallei: a prospective study in 1000 hospitalized children in northeast Thailand.

Throat swab cultures and indirect hemagglutination assay (IHA) for Pseudomonas pseudomallei were done in 1000 randomly selected children at a large hospital in northeast Thailand. During 18 months, 17 children with melioidosis were admitted (0.46% of pediatric admissions excluding neonates born in the hospital). Throat swab was positive for P. pseudomallei in 8 of these but in none of 1000 control children. IHA seroprevalence rose at a conversion rate of 24% per year, from 12% in those 1-6 months old to a plateau at approximately 80% after age 4 years. No control child < 4 had an IHA titer > 1:160. The median titer in children with melioidosis was 1:80 (range, negative [in3]-1:5120). Specificity of IHA declined with age, but high titers (> or = 1:640) remained diagnostically useful. Thus, throat carriage of P. pseudomallei indicates active melioidosis. There is no evidence for an asymptomatic carrier state in children. Environmental exposure to P. pseudomallei in endemic areas begins when the child becomes mobile.

Adolescent↗